Through the period from 4/1/76 experiments have primarily been designed to investigate the qualitative aspects of the research proposal, i.e., ultrastructural changes and alteration in the distribution of acid hydrolases in perfused rat hearts deprived of their oxygen as a result of decreased flow through the entire coronary arterial tree. The major findings of this study were as follows: Whole-heart ischemia was induced in isolated working rat hearts developing 75-90 mm Hg peak systolic pressures. A decline in peak systolic pressure to 30 mm Hg was chosen to represent ventricular failure. For light and electron microscopy, hearts were fixed after pressure development had decreased to 60 mm Hg and also 12 to 24 minutes after ventricular failure and compared to control hearts with normal coronary perfusion. Lysosomal activity was assessed using the Gomori reaction for the demonstration of acid phosphatase. 24 minutes after ventricular failure hearts showed a loss of glycogen stores, fragmentation of sarcomeres at the I band, disrupted sarcoplasmic reticulum and transverse tubules, vacuolization and decrease in matrix density of mitochondria, and separation of the intercalated disc at the level of the gap junctions. At 12 minutes the changes were more subtle. Ultrastructurally hearts appeared normal when fixed at peak systolic pressures of 60 mm of Hg. The Gomori reaction for the demonstration of acid phosphatase showed only occasional deposits of reaction product in association with residual bodies and primary lysosomes in the nuclear pole zone of myocardial cells from control hearts and hearts fixed at 60 mm Hg. Hearts examined 12 minutes after ventricular failure showed an increase in electron opaque precipitate in association with residual bodies, vesicular structures, and the Golgi apparatus. At 24 minutes after ventricular failure the localization of acid phosphatase was not as intense.